Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study, conducted over a time course of 36 hr after CCl4 administration, describes sequential morphometric and biochemical changes which occur in livers of rats exposed to a combination of low levels of chlordecone (10 ppm for 15 days) and a single ip injection of CCl4 (0.1 ml/kg). Those changes were compared to hepatic alterations which occur in rats that received the same dose of chlordecone or CCl4 alone. Biochemical studies showed only trivial increases in levels of glutamic-pyruvic transaminase (GPT), glutamic-oxalacetic transaminase (GOT), and moderate but temporary increases in isocitrate dehydrogenase (ICD) after CCl4 alone. The combination of chlordecone and CCl4 resulted in significantly greater elevations of all three serum enzymes at all time intervals examined. Morphometric data showed no difference between normal diet controls and animals exposed to chlordecone alone as far as numerical density of hepatocytes or volume densities of hepatocytes with glycogen, lipid, dilated rough endoplasmic reticulum (RER), pyknosis, or mitoses. Morphometric analysis of livers from animals that received CCl4 alone showed decreases in numerical density, temporary decrease in percentage of hepatocytes containing glycogen, an increase in hepatocytes containing lipid, temporary increase in hepatocytes with dilated RER, and temporary increases in pyknotic nuclei. Soon after the initial hepatic injury was histologically evident between 4 and 6 hr, the number of mitoses increased dramatically and this progressed until complete recovery from CCl4 damage. From all indices of damage, complete recovery was evident by 36 hr after CCl4 administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chlordecone-induced potentiation of carbon tetrachloride hepatotoxicity: a morphometric and biochemical study. 619 13

Orthotopic hepatic transplantation was performed upon 29 dogs. Four dogs received no immunosuppressant, 12 received cyclosporine and 13 received azathioprine. Dogs treated with cyclosporine at a dose of 20 milligrams per kilogram yielded histologic and functional data indistinguishable from those of the dogs in the sham transplant group. Histologic evidence of rejection consistently appeared when the dose was decreased to 10 milligrams per kilogram but was reversed upon resuming the administration of the higher dosage. Serum levels of bilirubin and hepatic enzymes, serum glutamic-oxalacetic transaminase, serum glutamic-pyruvic transaminase and alkaline phosphatase did not correlate with the development or resolution of histologic evidence of rejection in dogs receiving cyclosporine. Dogs receiving cyclosporine for 60 days had a prolonged survival when the drug was stopped, whereas the dogs receiving such therapy for less than 60 days did not have a prolonged survival period.
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PMID:Cyclosporine in transplantation of the liver in the dog. 634 81

As part of a six-month prospective study of the effects of neonatal thymectomy in the spontaneously diabetic BB Wistar rat, activities of the following enzymes were determined: alkaline phosphatase (AP), lactate dehydrogenase (LDH), creatine phosphokinase (CPK), glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT) and UDP-galactosyltransferase (UDPG). In prediabetics, AP and LDH levels were higher than in sham-operated, non-diabetic controls; however, this increase was seen in nearly all diabetes-prone BB rats, diminishing the usefulness of these changes in discerning potential diabetics from asymptomatic, diabetes-prone rats. After onset of the syndrome, there was a striking elevation of AP values in all diabetics with no similar alteration in asymptomatic, diabetes-prone rats suggesting this was a diabetes-related phenomenon. By contrast, UDPG was the only enzyme to decrease immediately following the onset of the syndrome. Both UDPG and AP levels correlated with blood glucose, the former negatively and the latter positively, suggesting a close relationship with changes occurring after onset of the syndrome. The remaining enzymes increased only in a portion of diabetics alone (GOT, GPT) or in a portion of both diabetics and asymptomatic, diabetes-prone BB rats (LDH, CPK).
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PMID:Serum enzymes in the BB rat before and after onset of the overt diabetic syndrome. 643 99

A total of 466 patients were treated with cefoperazone. The drug was usually administered by drip infusion of 2 to 4 gm/day. Therapy was described as markedly effective and moderately effective in 64 of 77 patients (83.1%) treated for urinary tract infections; 253 of 316 patients (80.1%) treated for respiratory infections; 37 of 48 patients (77.1%) treated for liver biliary duct infections; ten of 16 patients (62.5%) treated for septicemia; and seven of nine patients (77.8%) being treated for other infections. Overall, cefoperazone was effective 79.6% of all patients treated. With respect to bacteriological activity, the overall eradication rate for gram-negative organisms (including Pseudomonas aeruginosa, Klebsiella sp, Escherichia coli, Haemophilus influenzae, Enterobacter sp, and Proteus sp) was 81% (182/225) and for gram-positive (Staphyloccocus aureus, Streptococcus pneumoniae and Streptococcus faecalis) 90% (36/40). Of 205 patients who failed to respond to previous antibiotic therapy, 67.8% were treated effectively with cefoperazone. Side effects, such as skin eruption, pyrexia and diarrhea, occurred in only 4.8% of patients treated, while laboratory abnormalities, such as elevated glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, alkaline phosphatase, and eosinophil values, occurred in only 6.4% of the treated patients. None of these abnormal values were of clinical significance.
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PMID:Clinical trials with cefoperazone in the field of internal medicine in Japan. 644 92

The aim of this work is to evaluate the concentration of serum bile acids (SBA) as an index of impaired liver function in systemic lupus erythematosus (SLE) patients versus usual laboratory tests of hepato-biliary system diseases. In patients with SLE the mean fasting SBA concentration was 9.6 +/- 1.4 mumol/L; in normal subjects the concentration was 2.9 +/- 0.6 mumol/L (P less than 0.01). In patients with SLE, mean gamma-glutamyl transpeptidase (GGTP) concentration was 31.5 +/- 5.9 mU/ml versus 10.05 +/- 1.1 mU/ml in controls (P less than 0.01). The bromsulphalein (BSP) excretion test, 45 minutes after injection, was 6.8 +/- 1% in SLE patients versus 2.8 +/- 0.4% in controls (P less than 0.02). No significant difference was found between these two groups of subjects with respect to leucine aminopeptidase (LAP), alkaline phosphatase (AlPh), glutamic-oxalacetic transaminase (SGOT), glutamic-pyruvic transaminase (SGPT), bilirubin serum rates. SBA rate was abnormal in 50% of the SLE patients; GGTP rate and the BSP excretion test were abnormal in 38% and 27% respectively. Our findings show the presence of an actual liver impairment in SLE patients, significantly demonstrated by fasting SBA concentration, GGTP rate and BSP excretion test. Other liver function tests are less useful in evaluating hepatic damage in SLE.
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PMID:Concentration of serum bile acids as an index of hepatic damage in systemic lupus erythematosus. 646 63

Injectable progestogen, norethisterone enanthate (NET-EN, 200 mg/ml at 60 day intervals), was administered to 150 women for 2 years as their method of contraception. Blood levels of acid phosphatase, alkaline phosphatase, glutamate pyruvate transaminase, glutamate oxaloacetate transaminase, acetylcholinesterase (AChe), sialic acid were determined in all subjects to ascertain whether NET-EN therapy causes any adverse metabolic effect or damage to the functional status of the liver. NET-EN contraception did not alter the liver function enzymes but there is a significant increase (P0.001) in AChE activity after 2 years. Serum sialic acid level showed a transient increase up to 1 year, which however returned to control level later. The mechanism responsible for these changes and whether the rise in sialic acid and AChE activity are related to any pathological condition remain unclear at this stage.
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PMID:Studies on some enzymes and sialic acid during progestational contraceptive therapy. 646 44

Hepatic transport of indocyanine green (ICG) was examined in dogs chronically intoxicated with dimethylnitrosamine (DMN) (2 mg/kg) intraportally once a week for 6 weeks. In pathophysiological consequences, significant increases (p less than 0.05) were shown in both glutamic-pyruvic transaminase (GPT) and total plasma bile acids, but no significant difference was shown in body weight, liver wet weight, glutamic-oxaloacetic transaminase (GOT), plasma alkaline phosphatase activity, total plasma protein, and total plasma bilirubin. By histologic examination of livers from intoxicated dogs, increased fibrosis in periportal, perisinusoidal, and especially pericentral areas, with loss of normal architecture, was observed. Partial fibrous bridging between periportal and pericentral areas was also demonstrated, but extensive pseudolobulation with regenerative nodules was not observed. The portal venous pressure of the intoxicated dogs was increased by approximately 50% of that of control dogs. In intoxicated dogs, delays were shown in both plasma disappearance and biliary excretion of ICG and significant decreases were observed in the pharmacokinetic parameters k12 (plasma to liver transfer rate constant), V2 (distribution volume of liver compartment), and CLtot (total body-plasma clearance), while a significant increase was observed in k23 (intrahepatic diffusion and transport rate constant); the V1 (distribution volume of plasma compartment) was not altered. From these findings, it is suggested that the decrease in the intrinsic clearance of ICG for the hepatic uptake process might explain the decrease in ICG uptake rate into the liver which was observed in the DMN-intoxicated dogs. Dogs chronically intoxicated with DMN might be a good model for studying hepatic dysfunction.
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PMID:Hepatic transport of indocyanine green in dogs chronically intoxicated with dimethylnitrosamine. 647 62

The effect of nickel on cadmium nephro-toxicity and hepato-toxicity in rats was investigated. The administration of nickel (6 mg per kg, i.p., three days) or cadmium (6 mg per kg, i.m., once) significantly enhanced the urinary excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), amino acids, and proteins. In addition, it increased the activity of serum ALP, GOT, and glutamate pyruvate transaminase (GPT). These biochemical alterations in urine and serum were used as a measure of kidney and liver damage. Cadmium-induced enzymuria, proteinuria, amino aciduria and increase in the activity of serum enzymes were significantly less marked in animals pretreated with nickel than in controls. However, the accumulation of cadmium in kidneys and liver and its urinary excretion were unaffected by nickel pretreatment. The results suggest protection by nickel against cadmium nephro- and hepato-toxicity.
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PMID:Preventive effects of nickel on cadmium hepatotoxicity and nephrotoxicity. 647 83

To study the clinical course and biochemical features of congenital syphilitic hepatitis, the records of all 22 pediatric patients admitted to North Carolina Memorial Hospital between 1969 and 1979 with a positive maternal, cord blood, or serum VDRL were reviewed. Of the seven infants identified with symptomatic congenital syphilis, five had clinical and biochemical evidence of liver dysfunction. All five were jaundiced (peak bilirubin ranged from 8.4 to 29.8 mg/dl, in each case greater than 40% conjugated). Peak transaminase elevation ranged from seven to 150 times normal. Serum glutamic-oxaloacetic transaminase exceeded serum glutamic-pyruvic transaminase in each infant, the difference ranging to 7,400 U. The onset of illness did not occur until after treatment had been initiated in two of these five cases. Liver dysfunction increased with treatment in all four infants with serial enzyme determinations. Liver dysfunction also persisted for more than 6 weeks after adequate treatment in two cases. Liver biopsy 5 weeks after treatment in another infant showed giant cell hepatitis. These observations suggest that treatment can potentiate liver dysfunction in congenital syphilis and that viable treponemes are not necessarily essential in the pathogenesis of the hepatitis.
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PMID:Clinical manifestations of congenital syphilitic hepatitis: implications for pathogenesis. 648 65

The toxicity of 1-phenylcyclohexene (PC), a pyrolysis product of phencyclidine (PCP), and its interaction with PCP were evaluated. The ip LD50 of PC in Swiss male mice was 22 mmol/kg. Treatment of mice with PC at 2.2 mmol/kg/day, ip, for up to 7 days increased the liver/body weight ratio, which returned to normal within 7 days after PC withdrawal. Increases of 32% in serum glutamic-oxalacetic transaminase (SGOT) and 94% in serum glutamic-pyruvic transaminase (SGPT) were observed within 4 hr following the initial (Day 1) dose of PC. Smaller increases in the SGOT activity continued following Day 2 and 3 PC administrations. The SGPT activity remained elevated after these treatments. Activities of both enzymes, however, returned to normal within 24 hr following daily PC injections. No pathologic changes were observed in liver, brain, spleen, kidneys, and lungs with light microscopy. PC treatment for 4 days at 2.2 or 4.4 mmol/kg produced proliferation along with dilatation and fragmentation of the endoplasmic reticulum in liver. Scattering of ribosomes in the cytoplasm and dilatation of rough-surfaced cisternae were prominent at the higher dosage. Pretreatment of animals for 4 days with PC (1.1, 2.2, and 4.4 mmol/kg, ip) decreased pentobarbital- (60 mg/kg) induced sleeping time by 27, 64, and 80% and lowered PCP- (16.4 mumol/kg) stimulated locomotor activity by 18, 28, and 41%, respectively. Pretreatment of animals with PC for 1 hr inhibited (ED50: 2.3 mmol/kg) the PCP-induced locomotion. These results indicate that the PC treatment during a 7-day period produces some undesirable effects on liver function, which are reversible on its discontinuation. However, PC also weakens toxic effects of PCP.
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PMID:Toxicity of 1-phenylcyclohexene and its interaction with phencyclidine. 650 68


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